ArticleMolecular biology reports2014
Association between E23K variant in KCNJ11 gene and new-onset diabetes after liver transplantation.
Article in Molecular biology reports, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 11 papers.
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Who cites it
11 citing papers in PubMed, 19 citations in OpenAlex.
- Posttransplantation diabetes mellitus (PTDM): pharmacological aspects and genetic predispositions.Pharmacogenomics · 2024Review
- Single-nucleotide polymorphisms as important risk factors of diabetes among Middle East population.Human genomics · 2022Review
- Review
- A Time-Based Meta-Analysis on the Incidence of New Onset Diabetes after Liver Transplantation.Journal of clinical medicine · 2021Review
- Importance of genetic polymorphisms in liver transplantation outcomes.World journal of gastroenterology · 2020Review
- Evaluation of Angiotensinogen M235T and T174M Polymorphisms, Demographic and Clinical Factors in New-Onset Diabetes after Liver Transplantation in Iranian Patients.International journal of organ transplantation medicine · 2019Article
- Pharmacogenetics of posttransplant diabetes mellitus.The pharmacogenomics journal · 2017Review
- Genetic factors in pathogenesis of diabetes mellitus after kidney transplantation.Therapeutics and clinical risk management · 2017Review
- Post-Transplant Diabetes Mellitus: Causes, Treatment, and Impact on Outcomes.Endocrine reviews · 2016Review
- Polymorphism of Transcription Factor-7-Like 2 (TCF7L2) Gene and New-Onset Diabetes after Liver Transplantation.International journal of organ transplantation medicine · 2015Article
- Characterization of Remitting and Relapsing Hyperglycemia in Post-Renal-Transplant Recipients.PloS one · 2015Article
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Authors and funding
6 authors at 1 institution in 1 country.
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Abstract
New-onset diabetes after transplantation (NODAT) is an important complication after solid organ transplantation. NODAT is a polygenic disease and KCNJ11 E23K polymorphism is considered as a diabetes-susceptibility gene. The present study aimed to assess the association between KCNJ11 (rs5219) variants and the risk of developing NODAT after liver transplantation. This study was conducted on 120 liver transplant recipients who had received tacrolimus-based immunosuppressive drugs. The liver transplant recipients were divided into an new onset diabetes mellitus (NODM) and a non-NODM group. The NODAT group consisted of 60 patients who developed diabetes in the first 6 months after transplantation, while the non-NODAT group included 60 patients who remained euglycemic. The patients were genotyped using polymerase chain reaction-restriction fragment length polymorphism and the incidence of NODAT was compared between the two groups. Nongenetic risk factors including donor gender and cold ischemia time, and recipient (MELD score, presence of viral hepatitis, acute rejection and steroid pulse therapy) were also considered. The KCNJ11 KK variant was associated with an increased risk for NODAT with respective odds ratio of 6.03 (95 % confidence interval 2.37-15.4; P < 0.001]. Donor age and male sex, recipient age as well as fasting plasma glucose before transplantation were significantly different between NODAT and non-NODAT groups (P < 0.05). The prednisolone daily dosage was significantly higher in the NODAT group (P = 0.01). These patients received pulse of methyl prednisolone for treatment of acute rejection. This study showed that polymorphisms in KCNJ11 might predispose the patients treated by tacrolimus to development of NODAT after liver transplantation.
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